The present review provides an overview of the current knowledge of the potential immunomodulatory effects of vitamin D in the prevention of COVID?19 and sets out vitamin D recommendations for the Latin American population.Osteosarcoma (OS) is a musculoskeletal malignancy that originates from interstitial cells. An increasing number of studies have verified that long non?coding RNAs (lncRNAs) participate in the progression of numerous types of cancer. It has been reported that LINC00467 is a cancer?promoting gene in some types of cancer; however, the regulatory mechanism of LINC00467 in OS remains unknown. In the present study, reverse transcription-quantitative PCR was used to determine LINC00467 expression in OS tissues and cells. Additionally, the impact of LINC00467?knockdown on OS cell proliferation, migration and invasion was analyzed using Cell Counting Kit?8, colony formation and Transwell assays, as well as western blot analysis. RNA pulldown and luciferase reporter assays were conducted to investigate the regulatory mechanism of LINC00467 in OS. The results delineated that LINC00467 expression was elevated in OS tissues and cells, and that high LINC00467 expression was associated with a poor prognosis in patients with OS. LINC00467 inhibition suppressed OS progression by inhibiting cell proliferation, migration, invasion and epithelial?mesenchymal transition. LINC00467 served as a molecular sponge for microRNA (miR)?217, while karyopherin subunit α4 (KPNA4) was a downstream target gene of miR?217. Moreover, the overexpression of KPNA4 reversed the inhibitory effects of LINC00467 inhibition on OS progression. Therefore, the present study elucidated the potential mechanism of LINC00467 in OS and indicated that LINC00467 exerted its carcinogenic effects on OS through the miR?217/KPNA4 axis, implying that LINC00467 may be a novel potential therapeutic target for OS.MicroRNA?199a?3p (miR?199a?3p) is aberrantly expressed in various types of cancer where it exhibits a tumor suppressive role. However, the biological role of miR?199a?3p in ovarian cancer (OC) remains unclear. The present study aimed to investigate whether miR?199a?3p was a tumor suppressor in OC and to identify the possible mechanisms. It was found that miR?199a?3p expression was significantly downregulated in the tumor tissues and blood samples of patients with OC, as well as in three OC cell lines. In addition, its low expression was closely associated with International Federation of Gynecology and Obstetrics disease stage, histological grade and lymph node metastasis. It was demonstrated that overexpression of miR?199a?3p inhibited the viability and promoted apoptosis of OV90 and SKOV?3 cells. In addition, Yes?associated protein 1 (YAP1), a well?known oncogene, was identified as a direct target of miR?199a?3p in OC cells. Additionally, it was observed that YAP1 was significantly increased and inversely correlated with miR?199a?3p expression in OC tissues. Notably, YAP1 overexpression abrogated the tumor suppressive effects of miR?199a?3p in vitro. Collectively, the present results indicated that miR?199a?3p suppressed viability in OC cells, at least partly via inhibiting the YAP1 oncogene, suggesting that miR?199a?3p may act as a biomarker and therapeutic target for patients with OC.Endothelial dysfunction and diabetic vascular disease induced by chronic hyperglycemia involve complex interactions among high glucose, long non?coding RNAs (lncRNAs), microRNAs (miRNAs or miRs) and the Ser/Thr kinase AKT. However, the molecular mechanisms underlying the regulatory crosstalk between these have not yet been completely elucidated. Thus, the present study aimed to explore the molecular mechanisms whereby high glucose (HG)?induced lncRNA MIR181A2HG modulates human umbilical vein endothelial cell (HUVEC) proliferation and migration by regulating AKT2 expression. The persistent exposure of HUVECs to HG resulted in MIR181A2HG downregulation and thus reduced its ability to sponge miR?6832?5p, miR?6842?5p and miR?8056, subsequently leading to an increase in miR?6832?5p, miR?6842?5p and miR?8056 levels. Mechanistically, miR?6832?5p, miR?6842?5p and miR?8056 were found to target the 3'UTR of AKT2 mRNA in HUVECs, and the increase in their levels led to a decreased expression of AKT2. Thus, this also led to the suppression of HUVEC proliferation and migration, and the formation of capillary?like structures. Moreover, the suppression of HUVEC proliferation and migration induced by MIR181A2HG downregulation was accompanied by changes in glucose metabolism. On the whole, the present study demonstrates that the downregulation of lncRNA MIR181A2HG by HG impairs HUVEC proliferation and migration by dysregulating the miRNA/AKT2 axis. The MIR181A2HG/miRNA/AKT2 regulatory axis may thus be a potential therapeutic target for HG?induced endothelial dysfunction.Improving angiogenic capacity under hypoxic conditions is essential for improving the survival of skin grafts, as they often lack the necessary blood supply. The stable expression levels of hypoxia?inducible factor?1α (HIF?1α) in the nucleus directly affect the downstream vascular endothelial growth factor (VEGF) signaling pathway and regulate angiogenesis in a hypoxic environment. Astragaloside IV (AS?IV), an active component isolated from Astragalus membranaceus, has multiple biological effects including antioxidant and anti?diabetic effects, and the ability to provide protection from cardiovascular damage. However, the mechanisms underlying these effects have not previously been elucidated. The present study investigated whether AS?IV promotes angiogenesis via affecting the balance between ubiquitination and small ubiquitin?related modifier (SUMO) modification of HIF?1α. The results demonstrated that persistent hypoxia induces changes in expression levels of HIF?1α protein and significantly increases the proportion of dysplastic blood vessels. Further western blotting experiments showed that rapid attenuation and delayed compensation of SUMO1 activity is one of the reasons for the initial increase then decrease in HIF?1α levels. https://www.selleckchem.com/products/gsk583.html SUMO1 overexpression stabilized the presence of HIF?1α in the nucleus and decreased the extent of abnormal blood vessel morphology observed following hypoxia. AS?IV induces vascular endothelial cells to continuously produce SUMO1, stabilizes the HIF?1α/VEGF pathway and improves angiogenesis in hypoxic conditions. In summary, the present study confirmed that AS?IV stimulates vascular endothelial cells to continuously resupply SUMO1, stabilizes the presence of HIF?1α protein and improves angiogenesis in adverse hypoxic conditions, which may improve the success rate of flap graft surgery following trauma or burn.